Thesis: Ph. D., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, June 2016.Cataloged from PDF version of thesis.Includes bibliographical references (pages 51-56).This thesis addresses the question of how direction selectivity (DS) arises in the mouse retina. DS has long been observed in retinal ganglion cells, and more recently confirmed in the starburst amacrine cell. Upstream retinal bipolar cells, however, have been shown to lac, indicating that the mechanism that gives rise to DS lies in the inner plexiform layer, where the axons of bipolar cells costratify with amacrine and ganglion cells. We reconstructed a region of the IPL and identified cell types within it, and have discovered a mechanism which may explain the origin of DS activity in the mammalian retina, which relies on what we call "space-time wiring specificity." It has been suggested that a DS signal can arise from non-DS excitatory inputs if at least one among spatially segregated inputs transmits its signal with some delay, which we extend to consider also a difference in the degree to which the signal is sustained. Previously, it has been supposed that this delay occurs within the starburst amacrine cells' dendrites. We hypothesized an alternative, presynaptic mechanism. We observed that different bipolar cell types, which are believed to express different degrees of sustained activity, contact different regions of the starburst amacrine cell dendrite, giving rise to a space-time wiring specifity that should produce a DS signal. We additionally provide a model that predicts the strength of DS as a function of the spatial segregation of inputs and the temporal delay.by Matthew Greene.Ph. D.